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Prolactin (PRL) has been considered a key regulator of ion uptake in zebrafish. The genes  slc12a10.2  and  slc12a3 , which are Na +  and chloride Cl −  co-transporters, have been reported to be regulated by PRL in freshwater fish. The integrative network of PRL signaling dissected from the knockout of tissue-specific downstream PRL ion transporters remains poor. In the present study, zebrafish models with increased endogenous levels of PRL were generated through the knockout of  slc12a10.2  or  slc12a3 , and the developmental consequences were analyzed. The increased levels of pituitary PRL were observed in both  slc12a10.2 - and  slc12a3 -deficient fish. Unlike the  slc12a3 -deficient fish, which could survive to adulthood, the  slc12a10.2 -deficient fish began to die at 9 days post-fertilization (dpf) and did not survive beyond 17 dpf. This survival defect is a result of defective Cl −  uptake in this mutant, indicating that Slc12a10.2 plays an essential role in Cl −  uptake. Intriguingly, compared to the levels in control fish, no significant differences in the levels of Na +  in the body were observed in  slc12a10.2 - or  slc12a3 -deficient zebrafish. The upregulations of the PRL downstream transporters,  slc9a3.2, slc12a10.2 , and  atp1a1a.5  were observed in  slc12a3 -deficient fish in both the gills/skin and the pronephric duct. However, this type of response was not observed in the pronephric duct of  slc12a10.2 -deficient fish, except under Na + -deprived conditions. Our results show that PRL is susceptible to deficiencies in downstream ion transporters. Moreover, both the gills/skin and pronephric duct show differential expression of downstream PRL targets in response to increased levels of pituitary PRL caused by the depletion of tissue-specific ion transporters.

Depletion of Tissue-Specific Ion Transporters Causes Differential Expression of PRL Targets in Response to Increased Levels of Endogenous PRL